TY - JOUR
T1 - Altered Myocardial Shear Strains Are Associated With Chronic Ischemic Mitral Regurgitation
AU - Nguyen, Tom C.
AU - Cheng, Allen
AU - Langer, Frank
AU - Rodriguez, Filiberto
AU - Oakes, Robert A.
AU - Itoh, Akinobu
AU - Ennis, Daniel B.
AU - Liang, David
AU - Daughters, George T.
AU - Ingels, Neil B.
AU - Miller, D. Craig
N1 - Funding Information:
This work was supported by Grants HL-29589 and HL-67025 from the National Heart, Lung and Blood Institute. Doctors Nguyen, Langer, Cheng, Rodriguez, and Oakes were Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Doctors Nguyen and Cheng were recipients of the Thoracic Society Foundation Research Education (TSFRE) Fellowship Awards. Doctor Langer was also supported by the Deutsche Akademie der Naturforscher Leopoldina, Halle, Germany. Doctor Itoh was a recipient of the Uehara Memorial Foundation Research Fellowship. We deeply appreciate the technical expertise provided by Mary K. Zasio, BA, Maggie Brophy, AS, and Katha Gazda, BA. We thank Drs. James W. Covell, Andrew D. McCulloch, and Jeffrey H. Omens at the University of California, San Diego, and Dr. John C. Criscione at the Texas A&M University for their generous help and advice.
PY - 2007/1
Y1 - 2007/1
N2 - Background: Ischemic mitral regurgitation (IMR) limits life expectancy and can lead to postinfarction global left ventricular (LV) dilatation and remodeling, the pathogenesis of which is not completely known. We tested the hypothesis that IMR perturbs adjacent myocardial LV systolic strains. Methods: Thirteen sheep had three columns of miniature beads inserted across the lateral LV wall, with additional epicardial markers silhouetting the ventricle. One week later posterolateral infarction was created. Seven weeks thereafter, the animals were divided into two groups according to severity of IMR (≤ 1+, n = 7, IMR[-] vs ≥ 2+, n = 6, IMR[+]). Four dimensional marker coordinates and quantitative histology were used to calculate ventricular volumes, transmural myocardial systolic strains, and systolic fiber shortening. Results: Seven weeks after infarction, end-diastolic (ED) volume increased similarly in both groups, end-systolic (ES) E13 (circumferential-radial) shear increased in both groups, but more so in IMR(+) than IMR(-) (+0.12 vs 0.04, p < 0.005), and E12 (circumferential-longitudinal) shear increased in IMR(-) but not IMR(+) (+0.04 vs -0.01, p < 0.005). There were no significant differences in ED or ES remodeling strains or systolic fiber shortening between IMR(-) and IMR(+). Conclusions: An equivalent increase in LV end-diastolic (ED) volume in both groups, coupled with unchanged ED and end-systolic remodeling strains as well as systolic circumferential, longitudinal, and radial strains, argue against a global LV or regional myocardial geometric basis for the cardiomyopathy associated with IMR. Further, similar systolic fiber shortening in both groups militates against an intracellular (cardiomyocyte) mechanism. The differences in subepicardial E12 and E13 shears, however, suggest a causal role of altered interfiber (cytoskeleton and extracellular-matrix) interactions.
AB - Background: Ischemic mitral regurgitation (IMR) limits life expectancy and can lead to postinfarction global left ventricular (LV) dilatation and remodeling, the pathogenesis of which is not completely known. We tested the hypothesis that IMR perturbs adjacent myocardial LV systolic strains. Methods: Thirteen sheep had three columns of miniature beads inserted across the lateral LV wall, with additional epicardial markers silhouetting the ventricle. One week later posterolateral infarction was created. Seven weeks thereafter, the animals were divided into two groups according to severity of IMR (≤ 1+, n = 7, IMR[-] vs ≥ 2+, n = 6, IMR[+]). Four dimensional marker coordinates and quantitative histology were used to calculate ventricular volumes, transmural myocardial systolic strains, and systolic fiber shortening. Results: Seven weeks after infarction, end-diastolic (ED) volume increased similarly in both groups, end-systolic (ES) E13 (circumferential-radial) shear increased in both groups, but more so in IMR(+) than IMR(-) (+0.12 vs 0.04, p < 0.005), and E12 (circumferential-longitudinal) shear increased in IMR(-) but not IMR(+) (+0.04 vs -0.01, p < 0.005). There were no significant differences in ED or ES remodeling strains or systolic fiber shortening between IMR(-) and IMR(+). Conclusions: An equivalent increase in LV end-diastolic (ED) volume in both groups, coupled with unchanged ED and end-systolic remodeling strains as well as systolic circumferential, longitudinal, and radial strains, argue against a global LV or regional myocardial geometric basis for the cardiomyopathy associated with IMR. Further, similar systolic fiber shortening in both groups militates against an intracellular (cardiomyocyte) mechanism. The differences in subepicardial E12 and E13 shears, however, suggest a causal role of altered interfiber (cytoskeleton and extracellular-matrix) interactions.
UR - http://www.scopus.com/inward/record.url?scp=33845475248&partnerID=8YFLogxK
U2 - 10.1016/j.athoracsur.2006.08.039
DO - 10.1016/j.athoracsur.2006.08.039
M3 - Article
C2 - 17184629
AN - SCOPUS:33845475248
SN - 0003-4975
VL - 83
SP - 47
EP - 54
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
IS - 1
ER -